Senior Vice Chancellor's Research Seminar

Topic Overview:

Alzheimer’s disease (AD) is one of the most significant medical and societal challenges of our time. Several FDA-approved drugs can ameliorate some of the symptoms of AD, but no current intervention strategies can halt or modify the underlying disease mechanisms. Therefore, a major challenge is to gain a clearer understanding of the cellular processes that underlie disease pathogenesis in order to develop efficacious, mechanism-based therapeutic strategies for AD. Thathiah and colleagues address this challenge by using a multidisciplinary approach to understand the involvement of G protein-coupled receptors (GPCRs) in disease pathogenesis and to investigate the molecular mechanisms that link the two major disease hallmarks, namely amyloid-β (Aβ) to tau, to neurodegeneration in AD patients. Thathiah will discuss the identification and characterization of the orphan GPCR GPR3 in disease pathogenesis and ongoing research focused on understanding the crosstalk between Aβ and tau in disease progression.



Topic Overview: Alzheimer’s disease (AD) is one of the most significant medical and societal challenges of our time. Several FDA-approved drugs can ameliorate some of the symptoms of AD, but no current intervention strategies can halt or modify the underlying disease mechanisms. Therefore, a major challenge is to gain a clearer understanding of the cellular processes that underlie disease pathogenesis in order to develop efficacious, mechanism-based therapeutic strategies for AD. Thathiah and colleagues address this challenge by using a multidisciplinary approach to understand the involvement of G protein-coupled receptors (GPCRs) in disease pathogenesis and to investigate the molecular mechanisms that link the two major disease hallmarks, namely amyloid-β (Aβ) to tau, to neurodegeneration in AD patients. Thathiah will discuss the identification and characterization of the orphan GPCR GPR3 in disease pathogenesis and ongoing research focused on understanding the crosstalk between Aβ and tau in disease progression.